ArticleJournal of molecular neuroscience : MN2022
The Epigenetic Regulation of OLIG2 by Histone Demethylase KDM6B in Glioma Cells.
Article in Journal of molecular neuroscience : MN, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- KDM6B promotes VEGFA expression and vasculogenic mimicry in glioblastoma cells under hypoxia conditions.Experimental brain research · 2026Article
- Epigenetic Regulation of OLIG2 in Glioblastoma: Mechanisms and Therapeutic Targets to Combat Treatment Resistance.Journal of molecular neuroscience : MN · 2025Review
- The role of histone H3 lysine demethylases in glioblastoma.Cancer metastasis reviews · 2023Review
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Gliomas are common tumors that occur in the brain, accounting for 80% of all malignant brain tumors. Oligodendrocyte transcription factor 2 (OLIG2) is a key transcription factor and strongly expressed in gliomas, which drives proliferation and invasion of glioma cells. Our previous studies have shown that histone lysine (K) demethylase 6B (KDM6B) promotes glioma development. The data also showed that OLIG2 content was positively correlated with KDM6B. Based on this, we proposed that KDM6B may play biological roles by regulating OLIG2 expression. Subsequently, many experiments were performed including specific inhibitor treatment, gene knockdown, and chromatin immunoprecipitation (ChIP) array. These results indicated that inhibition of KDM6B enzymatic activity with GSK-J4 reduces OLIG2 gene expression and protein content. The KDM6B knockdown experiment yielded similar results, that is, it reduces the mRNA and protein level of OLIG2 in glioma cells. ChIP assay showed that the promoter of OLIG2 can be bound by KDM6B, which catalyzes the demethylation of H3K27me3 and increases the expression of OLIG2. This study reveals a new regulatory mechanism of OLIG2 by KDM6B, which has important implications for the future development of drugs for gliomas and other neurological diseases.
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Registered trials
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